Tardive dyskinesia is a late appearing side effect of prolonged treatment with neuroleptics. The condition is characterized by rhythmic constant movements of the tongue, lips and extremities, and frequently appears to be irreversible. Supersensitivity of central dopamine receptors has been proposed as the pathophysiologic mechanism. In preliminary work we hypothesized that relief from tardive symptoms might result from a period of over-stimulation of the supersensitive receptor. We therefore treated patients with 1-Dopa, which has been shown to increase central dopamine. We anticipated that initially there would be an increase in the severity of the dyskinesia, but that the receptor would adpat to the increased transmitter over time, and that clinical improvement would accompany withdrawal of the 1-Dopa. Patients were evaluated with clinical rating scales, quantitative measurement of digital tremor, and CCTV. Acute studies with physostigmine were done during the baseline period to better characterize the study population. Significant improvement in the dyskinesia was noted while tremography revealed lessening of tremor abnormalities, and the treatment appears clinically promising.